The Potential Mitigating Effect of Curcumin Root Extract Against Synthetic Anabolic Steroid Boldenone-Induced Kidney Injury in Male Rats

Background The anabolic-androgenic steroid boldenone is widely abused and is strongly linked to nephrotoxicity, primarily mediated through oxidative stress and inflammation. Curcumin, a natural polyphenol, is renowned for its potent antioxidant and anti-inflammatory properties, but its protective role against boldenone-induced renal injury is not fully elucidated. This study aimed to investigate the potential nephroprotective effects of curcumin against boldenone-induced kidney damage in a rat model, focusing on biochemical parameters, oxidative stress markers, inflammatory response, and histological changes. Methods Thirty-two male Wistar rats were divided into four groups (n=8): control, curcumin-only (300 mg/kg/day), boldenone-only (5 mg/kg/week), and boldenone + curcumin. Over the experimental period, body weight, kidney weight, food/water intake, and serum renal function markers (urea, creatinine, electrolytes) were monitored. Renal tissue was analyzed for oxidative stress markers (MDA, GSH, CAT, SOD), the inflammatory cytokine TNF-α, and histological alterations. Results Boldenone administration significantly increased body and kidney weights, serum urea, creatinine, potassium, and chloride, while decreasing sodium and calcium. It induced marked oxidative stress (elevated MDA, depleted GSH, CAT, SOD) and inflammation (elevated TNF-α), resulting in significant tubular necrosis and hypertrophy. Co-treatment with curcumin substantially mitigated these abnormalities, normalizing serum markers, restoring antioxidant defenses and electrolyte balance, reducing TNF-α expression, and ameliorating histological damage. Conclusion Curcumin exerts significant nephroprotection against boldenone-induced toxicity through its antioxidant, anti-inflammatory, and cytoprotective mechanisms. These findings justify its exploration as a potential adjunct therapy to prevent steroid-associated kidney injury. Future studies should focus on elucidating the precise molecular signaling pathways involved and validating these effects in clinical scenarios of AAS abuse.